 All right, well, go ahead and get started since it's 8 o'clock. I'm Tara Hahn, and I'm going to be presenting a case today. This is a 70-year-old male who originally presented to an outside provider for cataract surgery in his left eye. He presented with 2040 vision, IP in the mid-teens on three drops, superior altitudinal field loss, which was presumably from POAG, a primary open-angle glaucoma. And he underwent uncomplicated cataract surgery plus 180 degrees of AB interno canal glassy plus eye stint with intraoperative aberrometry to verify the lens power. On post-op week one, his IOP was quite low, 4 to 8 millimeters of mercury on his aqueous suppressant. So those were discontinued. And then on post-op day eight, he presented with an IOP spike of 40 and presented with significant pain in that eye. Despite starting maximum topical therapy and diamox, his IOP remained elevated over the next week. And his anterior chamber appeared more shallow than it did preoperatively. And then he also had quite a bit of a refractive surprise. So his target was minus 175, and he ended up as a minus 3. So after about a week of the diamox and aqueous suppressants, he was also started on cycloplegia in addition to these. And then his IOP dropped to the teens. But every time the referring physician tried to stop the cycloplegia, the IOP increased again to 30 to 35. The referring physician proceeded with an inferior and superior LPI. And yeah, it caps a lot of me to try to disturb the anterior hyalurid face. But this didn't help. So this isn't him, but say that it was. And he's presenting to you, as a second opinion, what would be on your differential? You can call on a resident on this one. This should be fairly straightforward. Guess by the title of my talk. He's Mr. Ray. Becca, you've already said it. He's Mr. Action. Just common things being common. It could be steroid induced glaucoma. So he initially had normal to low IOPs. And then he presented as an IOP spike on post op day 8. So a lot of times that's delayed. However, that usually responds to aqueous suppressants and diamox. So less likely to be that. It doesn't disappear with dilation. Right. And it could be pseudo exfoliation. They are notorious for having IOP spikes after any type of surgery, cataract surgery included. But usually those present more like on post op day 1 instead of post op week 1. And again, they respond to traditional management and not psychoplegia. It could be ankle closure with pupillary block. But again, wouldn't have responded to the PI. And oftentimes this doesn't really present after cataract surgery because you've created more space. So it's less likely. It could be super cordial hemorrhage. But again, that's less likely to present as a delayed presentation. More likely to be an intraoperative presentation and the referring physician did a dilated exam. Didn't see anything. It could be a choroidal mass or a choroidal effusion. Choroidal effusion doesn't quite fit because he would expect hypotony. He was hypotenuse at first, but usually doesn't lead to an increased pressure. But you would expect to see a flat chamber. And then finally, aqueous misdirection, which is what we thought that it was. So what is aqueous misdirection? So for whatever reason, and I'll go into some of the theories later, there is posteriorly directed aqueous formed here. And then instead of traversing the normal pathway for outflow, it gets directed posteriorly into the vitreous that causes positive posterior vitreous pressure and a flat anterior chamber because you have forward migration of the lens iris diaphragm. And once the angle becomes flat, then that leads to angle closure and then secondarily a rise in IOP. So this was originally described in 1869. It's also known as malignant glaucoma due to its progressive course and poor response to conventional therapy, but it's never really been thought to be associated with a malignancy, per se. And it's classically thought of as a complication of surgery for angle closure glaucoma. And early people who observed this thought that they saw anterior vitreous, anteriorly displaced as well as some clear, optically clear areas of aqueous within the vitreous. And interestingly, one of the earlier studies described a trial of lens extraction for aqueous misdirection. And it was only successful when there was vitreous loss in the cataract surgery, but an uncomplicated cataract surgery didn't fix the problem. So there's a lot of theories as to what's the inciting factor that causes this to happen. And I think we don't still completely know. One of the early theories was that there is posterior diversion of aqueous with accumulation behind a PVD, or posterior vitreous detachment, and that the anterior hyloid then acts kind of as a one-way valve that it lets fluid in, but then it gets trapped back here and it can't flow out. There was another theory that there's anterior hyloid obstruction from brakes in the hyloid near the vitreous space, a theory that there's lax lens annuals that kind of allows the anterior migration of the lens iris diaphragm. And then there's vitreous pressure leading to direct lens block. So the lens and ciliary body are what is actually blocking everything off. And it's sometimes referred to as a ciliary lenticular block as well. And then the most recent theory, right quickly, is that there is corroidal expansion after the surgery, which leads to an increased vitreous pressure, which then leads to vitreous compression. And so it's the decreased conductivity of atreus across the vitreous, which explains why the aqueous is originally allowed into the vitreous, and then it compresses and isn't allowed to kind of conduct itself back out. And so that there's a higher pressure posteriorly than anteriorly, and this kind of compounds on itself. The incidence is about 0.4 to 6% after an incisional glaucoma surgery, but it's also been reported after cataract surgery, retinal detachment, and even in cases of retinopathy of prematurity. Wrist factors include prior angle closure, the presence of peripheral anterior sneaky eye, axial hyperopia, especially in nanothalamus, and then over filtration at the time of glaucoma surgery. So all of the wrist factors kind of deal with having a shallow or flat anterior chamber as a predisposing factor to kind of allow this aqueousness direction to occur. So on presentations, patients present with pain, and then they'll have a diffusely shallow anterior chamber just like that picture I showed you. So there's no iris bombe as there is in pupillary block. It'll be as shallow peripherally as it is centrally, but with iris bombe you are more shallow peripherally than centrally. And they'll have normal to increase IOP. So the chamber may appear flat before the IOP rises. And then you have to exclude a choroidal effusion or super choroidal hemorrhage. And then the absence of pupillary block, which may require a PI to rule that out. And then patients will often have a myopic shift because they have an anteriorly displaced lens. And then on ultrasound bimicroscopy, they've shown that there is an anterior rotation of the ciliary body and forward rotation of the lens iris diaphragm, which resolves with treatment. And this was a study, which was the largest study that I could find of risk factors of malignant glaucoma after glaucoma surgery. So it was 1,689 patients. It was a retrospective review of patients undergoing various types of glaucoma surgery. And it was either done with FACO or without FACO. And I thought this was interesting. The meantime from surgery to aqueousness direction was 61 days, which is a lot longer than I thought it would be. And then the incidence after penetrating glaucoma surgery was 2.3% in their study. And they had no cases of aqueousness direction after non-penetrating surgery, which they defined as basically mig. So ice stance, eyepass, viscocanolostomy, or canaloplasty. And they found that shallow, preoperative shallow urtocornial angle was a significant risk factor. And they had defined that as zero to 20 degrees based on the Schaefer classification. And there was no difference in the type of glaucoma surgery. So as obviously non-penetrating surgery wasn't a risk factor, but any of the penetrating surgery, they didn't find any significant difference between the types. So medical treatment consists of cycliclegia. And that's important to try to posteriorly displace the lens iris diaphragm. And in patients who medical treatment is successful, that should be the last thing that you withdraw. Aqueous suppression, hyper-osmotic agents, and this is successful in 50% of patients within five days. And then in the 50% of patients where that's not successful, you can first try a YAG PI to distur, and then also use the YAG to try to disturb the interior vitreous base, or interior hyaloid face, but that's really only possible in a pseudophagic patient. And then this urtocornular hyaloidotomy or hyaloid vitrectomy, which I'll go into a little bit more in detail, but basically you're trying to create a unicameral eye where you're creating either a laser PI or urototomy, and then disturbing the same area through the zonules, and then also creating a communication with the anterior hyaloid. And removal of the anterior vitreous is key. It's not necessarily that you need all of the vitreous to be removed, but removing the anterior vitreous is kind of the pathologic part of this syndrome. In one study they looked at core protractomy as a treatment for these patients, and they found it to be only successful in 25 to 50% of fake egg eyes, but successful in 65 to 90% of pseudophagic eyes, and that's not that in fake egg eyes, you're not really safely able to get to the anterior vitreous, so that remains behind, and in pseudophagic eyes, you are able to remove that anterior vitreous. And then for fake egg eyes, surgical management includes cataract extraction plus the IZH. And this is kind of a flow diagram just discussing everything that I talked about. So first you'll start with medical therapy. If it's a pseudophagic or a fake egg patient, you can do a PI and try to also disturb the hyaloid face. I think this is kind of controversial. Some people would skip this step and then go straight to the IZH procedure. And then if it's a fake egg patient, you can try a PI to make sure that it's not pupillary walk, but then ultimately the treatment is going to be cataract extraction plus IZH. And the surgery can be done through the traditional way that we think of with vitrectomy pars plana, or it can be done through a clear pointial incision as an anterior ear approach, and I'll show you some examples of that. So this is our patient. So two paracentesi, or three paracentesis have been made. And now Dr. Crandall is going through the capsule, through the zonules to access the anterior vitreous with the vitrector. And now he's under the lens optic in the vitreous doing a limited vitrectomy. This is a previous cataract surgery or at the time of? This was a previous cataract surgery that presented with aqueous misdirection later on. Yeah, the cataract surgery was done outside. This patient already had a Yag laser capsule on him? Correct, yes. Already had Yag PI and capsule otomy. And so then injected myocall, and then he's creating an iridotomy with a vitrector in that same area where he did the anterior vitrectomy to try to create a communication so that it's a unicameral eye. And this is another video from a technique paper where they're creating, again, The NVR blade is used for the corneal incision which passes through the cornea, the iris, the zonules, And here he's using an NVR blade to make the PI. So he created like a peripheral opening in the iris. And then using the anterior vitrector to actually go through the iridotomy that he created to access the vitreous. I think this probably results in a larger opening in the iris. And then they do an anterior vitrectomy and inject triessence to make sure there's no vitreous remaining and suture the wound. The benefit of the anterior approach is that you are theoretically preserving the contractiva if they need a future filtering surgery. As many of these patients might if it's refractory to the first treatment. So, and what about the treatment of the fellow eye? So if the angle is occludable, it's reasonable to proceed with prophylactic PI. You definitely wanna avoid the use of myotics. And then after surgery, consider cycloclegia and also consider prophylactic vitrectomy depending on the course in the first eye. So if it was really refractory to medical treatment and didn't have a good outcome, it may be something that, and if their angle was shallow to begin with and the type of surgery that you're doing is high risk, you may consider that. This is just a table showing a lot of different reviews in the literature, or sorry, case series in the literature that have done some version of the IZH procedure and that most of the time it is successful in restoring the anatomy of the eye. In our case, on post-op day one, his pressure was 22, his anterior chamber was deeper than preoperatively and he had been taken off his dimox and cycloclegia after the surgery. And here's his UBM. So you can see the lens iris diaphragm is in the right position and it's not migrated anteriorly. His iridotomy is open. The anterior chamber appears nice and deep. So in summary, aqueous misdirection, also known as mollignit glaucoma, sometimes known as ciliary glaucoma, is a condition following surgery where aqueous becomes misdirected posteriorly, causing a forward displacement of the lens iris diaphragm. Aqueous most commonly following incisional glaucoma surgery. Risk factors include angle closure, glaucoma, hyperopia and a narrow angle. Signs include diffusely shallow anterior chamber, high IOP in the absence of pupillary block and they can also get a myopic shift. And then medical treatment includes cycloclegia and aqueous suppressants and surgical treatments includes iridozontal or hyaloid protracting. Questions? You rule for osmotics in the years later? Oh, yeah, definitely that's recommended. And the idea is if the pathologic process is that the vitreous is becoming more contracted and not allowing aqueous to be conducted back through it to get out through the normal outflow pathways that osmotics might allow the vitreous to become less contracted. So that's part of the medical therapy is aqueous suppressants. I don't think this gentleman got Manitola originally but that would have been a good idea to try. The other reason is it's often hard to get the pressure down at all and if you operate on a really high pressure aisle you really increase your risk of hemorrhage. Yeah. So you want to definitely what you need to get the pressure down to a reasonable level as you open that eye. Also remember as we do this, I don't get where our retinal surgeons here, they've always been nervous that as we're going out through the zonular area that we're working around the vitreous base and we've got to be pretty careful because that's a place where you can easily create a tear in the retina. And the other thing to remember is is because it's a partial protractomy is if you're coming back out and there's any sense that vitreous is following you, if it plugs that area up you're going to be right back where you started. So you've got to make sure there's nothing but aqueous flowing through that area. I've seen both of those errors in my career. Any thoughts from the retina people? Tara, I'm sure they have lots of thoughts. They're just pondering what they might be. Tara, what did you find as the percentage, I don't know if you came across it of these aqueous misdirection cases that would resolve a loan just with conservative management, cycloplasia and steroids? What I read was 50% within five days. So give it five days on conservative management. And I think you could try longer but the thought is that about half will resolve a loan and that they may need to be on cycloplasia for like a very, very long time. And that's the last thing that you're going to withdraw. So withdraw the aqueous suppressants, hypothermotic agents and then last the cycloplasia. Was there a recurrence percentage? I didn't see that. But I imagined that probably in a lot of them when you try to withdraw the cycloplasia and that's kind of what happened in this case. It was working with this cycloplasia but every time they tried to withdraw it, it came back.